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      Extreme βHCG levels in first trimester screening are risk factors for adverse maternal and fetal outcomes

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          Abstract

          Multiples of the normal median (MoM) of free βHCG is a valuable parameter in evaluation of risk of adverse pregnancy outcomes. In the current retrospective study, we assessed the maternal and fetal outcomes in pregnant women having free βHCG MoM levels < 0.2 or > 5 in their first trimester screening (FTS). Relative risk of trisomy 21 was significantly higher in patients having free βHCG MoM > 5. On the other hand, relative risk of trisomies 13 and 18 and Turner syndrome were higher in those having free βHCG MoM < 0.2. Other chromosomal abnormalities were nearly equally detected between those having free βHCG MoM < 0.2 or > 5. Relative risk of hydrocephaly and hydrops fetalis was higher when free βHCG MoM was below 0.2. On the other hand, relative risk of low birth weight was higher when free βHCG MoM was above 5. Moreover, frequency of gestational diabetes mellitus, preeclampsia, preterm delivery and vaginal bleeding increased with levels of free βHCG MoM. However, polyhydramnios had the opposite trend. Frequencies of premature rupture of membranes and pregnancy induced hypertension were highest among pregnant women having levels of free βHCG MoM < 0.2. The current study indicates importance of free βHCG MoM in identification of at-risk pregnancies in terms of both fetal and maternal outcomes. In fact, βHCG MoM < 0.2 or > 5 can be regarded as risk factors for adverse maternal or fetal outcomes irrespective of the presence of other abnormalities in the FTS results.

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          Biological functions of hCG and hCG-related molecules

          Laurence A. Cole (2010)
          Background hCG is a term referring to 4 independent molecules, each produced by separate cells and each having completely separate functions. These are hCG produced by villous syncytiotrophoblast cells, hyperglycosylated hCG produced by cytotrophoblast cells, free beta-subunit made by multiple primary non-trophoblastic malignancies, and pituitary hCG made by the gonadotrope cells of the anterior pituitary. Results and discussion hCG has numerous functions. hCG promotes progesterone production by corpus luteal cells; promotes angiogenesis in uterine vasculature; promoted the fusion of cytotrophoblast cell and differentiation to make syncytiotrophoblast cells; causes the blockage of any immune or macrophage action by mother on foreign invading placental cells; causes uterine growth parallel to fetal growth; suppresses any myometrial contractions during the course of pregnancy; causes growth and differentiation of the umbilical cord; signals the endometrium about forthcoming implantation; acts on receptor in mother's brain causing hyperemesis gravidarum, and seemingly promotes growth of fetal organs during pregnancy. Hyperglycosylated hCG functions to promote growth of cytotrophoblast cells and invasion by these cells, as occurs in implantation of pregnancy, and growth and invasion by choriocarcinoma cells. hCG free beta-subunit is produced by numerous non-trophoblastic malignancies of different primaries. The detection of free beta-subunit in these malignancies is generally considered a sign of poor prognosis. The free beta-subunit blocks apoptosis in cancer cells and promotes the growth and malignancy of the cancer. Pituitary hCG is a sulfated variant of hCG produced at low levels during the menstrual cycle. Pituitary hCG seems to mimic luteinizing hormone actions during the menstrual cycle.
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            First trimester maternal serum free beta human chorionic gonadotrophin and pregnancy associated plasma protein A as predictors of pregnancy complications.

            S Munim, Steven Spencer, W Liao … (2000)
            To examine the value of first trimester maternal serum free beta human chorionic gonadotrophin (beta hCG) and pregnancy associated plasma protein A (PAPP-A) as predictors of pregnancy complications. Screening study. Antenatal clinics. Singleton pregnancies at 10-14 weeks of gestation. Maternal serum free beta hCG and PAPP-A were measured at 10-14 weeks of gestation in 5,584 singleton pregnancies. In the 5,297 (94.9%) pregnancies with complete follow up free beta hCG and PAPP-A were compared between those with normal outcome and those resulting in miscarriage, spontaneous preterm delivery, pregnancy induced hypertension or fetal growth restriction and in those with pre-existing or gestational diabetes. Maternal serum PAPP-A increased and beta hCG decreased with gestation. The multiple of median maternal serum PAPP-A was significantly lower in those pregnancies resulting in miscarriage, pregnancy induced hypertension, growth restriction and in those with pre-existing or gestational diabetes mellitus, but not in those complicated by spontaneous preterm delivery. The level was < 10th centile of the reference range in about 20% of the pregnancies that subsequently resulted in miscarriage or developed pregnancy induced hypertension or growth restriction, and in 27% of those that developed gestational diabetes. Maternal serum free beta hCG was < 10th centile of the reference range in about 15% of the pregnancies that subsequently resulted in miscarriage or developed pregnancy induced hypertension or growth restriction, and in 20% of those that developed gestational diabetes. Low maternal serum PAPP-A or beta hCG at 10-14 weeks of gestation are associated with subsequent development of pregnancy complications.
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              Molecular pathways disrupted by gestational diabetes mellitus

              Caitlyn Nguyen-Ngo, Nanthini Jayabalan, Carlos Salomon … (2019)
              Gestational diabetes mellitus (GDM) imposes serious short- and long-term health problems for mother and baby. An effective therapeutic that can reduce the incidence of GDM and improve long-term maternal and fetal outcomes is a major research priority, crucially important for public health. A lack of knowledge about the underlying pathophysiology of GDM has hampered the development of such therapeutics. What we do know, however, is that maternal insulin resistance, low-grade inflammation and endothelial cell dysfunction are three central features of pregnancies complicated by GDM. Indeed, data generated over the past decade have implicated a number of candidate regulators of insulin resistance, inflammation and endothelial cell dysfunction in placenta, maternal adipose tissue and skeletal muscle. These include nuclear factor-κB (NF-κB), peroxisome proliferator-activated receptors (PPARs), sirtuins (SIRTs), 5′ AMP-activated protein kinase (AMPK), glycogen synthase kinase 3 (GSK3), PI3K/mTOR, inflammasome and endoplasmic reticulum (ER) stress. In this review, the identification of these as key modulators of GDM will be discussed. The biochemical pathways involved in the formation of these may represent potential sites for intervention that may translate to therapeutic interventions to prevent the development of GDM.
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                Author and article information

                Contributors
                Soudeh Ghafouri-Fard: s.ghafourifard@sbmu.ac.ir
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 21 January 2023
                Publication date PMC-release: 21 January 2023
                Publication date Collection: 2023
                Volume: 13
                Electronic Location Identifier: 1228
                Affiliations
                [1 ]Nilou Laboratory, Tehran, Iran
                [2 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, Tehran University of Medical Sciences, ; Tehran, Iran
                [3 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, Department of Medical Genetics, School of Medicine, , Tehran University of Medical Sciences, ; Tehran, Iran
                [4 ]GRID grid.411600.2, Department of Medical Genetics, , Shahid Beheshti University of Medical Sciences, ; Tehran, Iran
                Article
                Publisher ID: 28561
                DOI: 10.1038/s41598-023-28561-9
                PMC ID: 9867730
                PubMed ID: 36681713
                SO-VID: 9b916531-8998-43f7-912b-8e1836372597
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 24 August 2022
                Date accepted : 20 January 2023
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2023

                ScienceOpen disciplines: Uncategorized
                Keywords: biochemistry,genetics,biomarkers
                Data availability:
                ScienceOpen disciplines: Uncategorized
                Keywords: biochemistry, genetics, biomarkers

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